自噬
活性氧
机制(生物学)
平衡
心肌病
缺血
细胞生物学
生物
铁稳态
核受体
新陈代谢
癌症研究
医学
神经科学
生物信息学
生物化学
转录因子
内科学
心力衰竭
基因
细胞凋亡
哲学
认识论
作者
Xuemei Jin,Chunjie Jiang,Zhizhou Zou,He Huang,Xiaojian Li,Songji Xu,Rongshao Tan
标识
DOI:10.1016/j.jnutbio.2023.109339
摘要
Iron is an essential trace element that is involved in a variety of physiological processes. Ferritinophagy is selective autophagy mediated by nuclear receptor coactivator 4 (NCOA4), which regulates iron homeostasis in the body. Upon iron depletion or starvation, ferritinophagy is activated, releasing large amounts of Fe2+ and increasing reactive oxygen species (ROS), leading to ferroptosis. This plays a significant role in the etiopathogenesis of many diseases, such as metabolic diseases, neurodegenerative diseases, infectious diseases, tumors, cardiomyopathy, and ischemia-reperfusion ischemia-reperfusion injury. Here, we first review the regulation and functions of ferritinophagy and then describe its involvement in different diseases, with hopes of providing new understanding and insights into iron metabolism and iron disorder-related diseases and the therapeutic opportunity for targeting ferritinophagy.
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